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Nonmuscle myosin IIA promotes the internalization of influenza A virus and regulates viral polymerase activity through interacting with nucleoprotein in human pulmonary cells

查看全文 作　　者：Jian [1,2,3]Chen;Jian [3]Liu;Zhilu [3]Chen;Daobin [3]Feng;Cuisong [3]Zhu;Jun [3]Fan;Shuye [1,3]Zhang;Xiaoyan [1,3]Zhang;Jianqing [1,3]Xu 高影响力作者 机构地区：[1]Clinical Center for Bio-Therapy,Zhongshan Hospital,Fudan University(Xiamen Branch),Shanghai,200032,China;[2]Center for Infectious Disease Research,Science of Life Sciences,Westlake University,Hangzhou,310024,China;[3]Shanghai Public Health Clinical Center&Institutes of Biomedical Sciences,Shanghai Medical College,Fudan University,Shanghai,201508,China高影响力机构 出　　处：《Virologica Sinica》索引2023年第38卷第1期,共14页高影响力期刊 基　　金：supported by the National Natural Science Foundation of China(82071788,81901598,81771704,and 82041015);National Key R&D Program of China(2022YFC2604100). 摘　　要：Influenza A virus(IAV),responsible for seasonal epidemics and recurring pandemics,represents a global threat to public health.Given the risk of a potential IAV pandemic,it is increasingly important to better understand virushost interactions and develop new anti-viral strategies.Here,we reported nonmuscle myosin IIA(MYH9)-mediated regulation of IAV infection.MYH9 depletion caused a profound inhibition of IAV infection by reducing viral attachment and internalization in human lung epithelial cells.Surprisingly,overexpression of MYH9 also led to a significant reduction in viral productive infection.Interestingly,overexpression of MYH9 retained viral attachment,internalization,or uncoating,but suppressed the viral ribonucleoprotein(vRNP)activity in a minigenome system.Further analyses found that excess MYH9 might interrupt the formation of vRNP by interacting with the viral nucleoprotein(NP)and result in the reduction of the completed vRNP in the nucleus,thereby inhibiting subsequent viral RNA transcription and replication.Together,we discovered that MYH9 can interact with IAV NP protein and engage in the regulation of vRNP complexes,thereby involving viral replication.These findings enlighten new mechanistic insights into the complicated interface of host-IAV interactions,ultimately making it an attractive target for the generation of antiviral drugs. 关 键 词：Myosin IIA(MYH9) Influenza A virus(IAV) vRNP activity Virus-host interactions Virus entry
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